Evidence map›Paper›PMID 35608339›Full record

ReviewThe Biochemical journal2022

No longer married to inflammasome signaling: the diverse interacting pathways leading to pyroptotic cell death.

Ashley Weir, James E Vince

Open access · hybridAbstract readReview
In one paragraph

Review in The Biochemical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. The PANoptosis hypothesis examined.Nature reviews. Molecular cell biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Copper and vanadium induce oxidative stress and pyroptosis in the duck brain via activating the TLR4/NF-κB-p65 signaling pathway.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Gasdermins and pyroptosis in the kidney.Nature reviews. Nephrology · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Ashley WeirThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia.
James E VinceThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia.ORCID 0000-0001-7166-2798
The University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For over 15 years the lytic cell death termed pyroptosis was defined by its dependency on the inflammatory caspase, caspase-1, which, upon pathogen sensing, is activated by innate immune cytoplasmic protein complexes known as inflammasomes. However, this definition of pyroptosis changed when the pore-forming protein gasdermin D (GSDMD) was identified as the caspase-1 (and caspase-11) substrate required to mediate pyroptotic cell death. Consequently, pyroptosis has been redefined as a gasdermin-dependent cell death. Studies now show that, upon liberation of the N-terminal domain, five gasdermin family members, GSDMA, GSDMB, GSDMC, GSDMD and GSDME can all form plasma membrane pores to induce pyroptosis. Here, we review recent research into the diverse stimuli and cell death signaling pathways involved in the activation of gasdermins; death and toll-like receptor triggered caspase-8 activation of GSDMD or GSMDC, apoptotic caspase-3 activation of GSDME, perforin-granzyme A activation of GSDMB, and bacterial protease activation of GSDMA. We highlight findings that have begun to unravel the physiological situations and disease states that result from gasdermin signaling downstream of inflammasome activation, death receptor and mitochondrial apoptosis, and necroptosis. This new era in cell death research therefore holds significant promise in identifying how distinct, yet often networked, pyroptotic cell death pathways might be manipulated for therapeutic benefit to treat a range of malignant conditions associated with inflammation, infection and cancer.

Indexed as

InflammasomesPyroptosisCaspase 1CaspasesPhosphate-Binding ProteinsCaspase 1CaspasesInflammasomesPhosphate-Binding ProteinsapoptosisgasderminGSDMDinflammasomenecroptosispyroptosis

Identifiers

PMID35608339
PMCPMC9162454
OpenAlexW4281556855

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.